Hepatic glycerol flux after E. coli endotoxin administration

1984 ◽  
Vol 247 (4) ◽  
pp. R687-R692 ◽  
Author(s):  
O. P. McGuinness ◽  
J. J. Spitzer
Keyword(s):  
Blood Flow ◽  
Clearance Rate ◽  
Arterial Blood Flow ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Metabolic Clearance Rate ◽  
Endotoxin Administration ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Glucose Output

Hepatic glycerol flux was examined in dogs after the administration of Escherichia coli endotoxin (0.4 mg/kg) to determine the contribution of the liver to the previously observed decline in the metabolic clearance rate of glycerol. Hepatic glycerol flux was estimated by determining hepatic arterial and portal venous blood flows with electromagnetic flow probes and by measuring arteriovenous difference of glycerol across the liver. Administration of endotoxin significantly decreased total hepatic blood flow (by approximately 20%) but did not alter hepatic arterial blood flow. Hepatic glycerol clearance decreased by 25–30% after endotoxin administration. Hepatic glycerol extraction also decreased. Under control conditions, 60% of the metabolic clearance rate of glycerol was attributable to the liver, whereas in the postendotoxin state approximately 72% of the glycerol clearance could be accounted for by hepatic clearance. Thus changes in transhepatic glycerol flux are only partially responsible for the previously observed alterations in glycerol clearance after endotoxin administration. Although hepatic glycerol clearance decreased, net hepatic glycerol, as well as lactate and alanine, uptake did not decrease, indicating that gluconeogenic precursor availability to the hepatocytes was not diminished. Hepatic glucose output was elevated after endotoxin administration. Changes in hepatic glucose output and gluconeogenic precursor uptake help explain the endotoxin-induced alternations in the fluxes of these metabolites.

Hepatic lactate uptake versus leg lactate output during exercise in humans

2007 ◽  
Vol 103 (4) ◽  
pp. 1227-1233 ◽  
Author(s):  
H. B. Nielsen ◽  
M. A. Febbraio ◽  
P. Ott ◽  
P. Krustrup ◽  
N. H. Secher
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Prolonged Exercise ◽  
Incremental Exercise ◽  
Hepatic Glucose Output ◽  
Arterial Lactate ◽  
Hepatic Glucose ◽  
Lactate Output ◽  
Lactate Uptake ◽  
Glucose Output

The exponential rise in blood lactate with exercise intensity may be influenced by hepatic lactate uptake. We compared muscle-derived lactate to the hepatic elimination during 2 h prolonged cycling (62 ± 4% of maximal O2 uptake, V̇o2max) followed by incremental exercise in seven healthy men. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermodilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 ± 0.5 vs. 6.5 ± 0.6 mmol/min; mean ± SE) and at an arterial lactate of 2.0 ± 0.2 mM, the leg lactate output of 3.0 ± 1.8 mmol/min was about fourfold higher than the hepatic lactate uptake (0.7 ± 0.3 mmol/min). During incremental exercise, the hepatic glucose output was about one-third of the leg glucose uptake (2.0 ± 0.4 vs. 6.2 ± 1.3 mmol/min) and the arterial lactate reached 6.0 ± 1.1 mM because the leg lactate output of 8.9 ± 2.7 mmol/min was markedly higher than the lactate taken up by the liver (1.1 ± 0.6 mmol/min). Compared with prolonged exercise, the hepatic lactate uptake increased during incremental exercise, but the relative hepatic lactate uptake decreased to about one-tenth of the lactate released by the legs. This drop in relative hepatic lactate extraction may contribute to the increase in arterial lactate during intense exercise.

scholarly journals Unlike mice, dogs exhibit effective glucoregulation during low-dose portal and peripheral glucose infusion

2004 ◽  
Vol 286 (2) ◽  
pp. E226-E233 ◽  
Author(s):  
Mary Courtney Moore ◽  
Sylvain Cardin ◽  
Dale S. Edgerton ◽  
Ben Farmer ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Low Dose ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Hepatic Glucose Output ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Arterial Blood Glucose ◽  
Hepatic Portal ◽  
Glucose Output ◽  
Arteriovenous Difference

Portal infusion of glucose in the mouse at a rate equivalent to basal endogenous glucose production causes hypoglycemia, whereas peripheral infusion at the same rate causes significant hyperglycemia. We used tracer and arteriovenous difference techniques in conscious 42-h-fasted dogs to determine their response to the same treatments. The studies consisted of three periods: equilibration (100 min), basal (40 min), and experimental (180 min), during which glucose was infused at 13.7 μmol· kg–1·min–1 into a peripheral vein (PE, n = 5) or the hepatic portal (PO, n = 5) vein. Arterial blood glucose increased ∼0.8 mmol/l in both groups. Arterial and hepatic sinusoidal insulin concentrations were not significantly different between groups. PE exhibited an increase in nonhepatic glucose uptake (non-HGU; Δ8.6 ± 1.2 μmol·kg–1·min–1) within 30 min, whereas PO showed a slight suppression (Δ–3.7 ± 3.1 μmol·kg–1·min–1). PO shifted from net hepatic glucose output (NHGO) to uptake (NHGU; 2.5 ± 2.8 μmol·kg–1·min–1) within 30 min, but PE still exhibited NHGO (6.0 ± 1.9 μmol·kg–1·min–1) at that time and did not initiate NHGU until after 90 min. Glucose rates of appearance and disappearance did not differ between groups. The response to the two infusion routes was markedly different. Peripheral infusion caused a rapid enhancement of non-HGU, whereas portal delivery quickly activated NHGU. As a result, both groups maintained near-euglycemia. The dog glucoregulates more rigorously than the mouse in response to both portal and peripheral glucose delivery.

Effect of Catecholamines and Dibutyryl-cyclic-AMP on Glucose Turnover, Plasma Free Fatty Acids, and Insulin in Dogs Treated with Methylprednisolone

1972 ◽  
Vol 50 (10) ◽  
pp. 999-1006 ◽  
Author(s):  
Bela Issekutz Jr. ◽  
Ingrid Borkow
Keyword(s):  
Cyclic Amp ◽  
Treated Group ◽  
Glucose Turnover ◽  
Immunoreactive Insulin ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Lactate Levels ◽  
Glucose Output ◽  
Hyperglycemic Effect

The turnover rate of glucose was measured in dogs with indwelling arterial and venous catheters, according to the primed constant rate infusion techniques, using 2-3H-glucose as tracer. The effects of adrenalin (A), noradrenalin (NA), and dibutyryl-cAMP (DBcAMP) infusions were tested on normal dogs and on dogs treated for 3 days with methylprednisolone (MP, 3–3.5 mg/kg day). MP potentiated the hyperglycemic effect of A (0.5 μg/kg min) six- to sevenfold, and the increase of hepatic glucose output (Ra) 11-fold. In addition, the free fatty acid (FFA) increasing and lactacidemic effects of A were significantly potentiated by MP. A prevented the rise of immunoreactive insulin even though plasma glucose reached values of 400–450 mg%. The metabolic clearance rate was significantly decreased by A. NA (0.5 μg/kg min) had no hyperglycemic effect in the controls, but it increased the blood sugar by 120 mg% in the treated group. This was caused by a more than twofold increase in the hepatic glucose output. MP treatment did not alter the NA induced rise of FFA and no effect was seen on plasma lactate levels. NA caused a transient rise of insulin in the controls and a greater and more sustained one in treated dogs. Following MP treatment, DBcAMP (0.1 or 0.2 mg/kg min) also caused a much greater hepatic glucose output and hyperglycemia than what had been obtained on the same animals prior to treatment. DBcAMP increased plasma insulin and decreased FFA. It is concluded that the cyclic-AMP sensitivity of hepatic enzyme systems involved in glucose output was greatly increased by MP treatment.

The Kinetics of Plasma Noradrenaline in Normal and Hypertensive Subjects

1978 ◽  
Vol 55 (s4) ◽  
pp. 89s-92s ◽  
Author(s):  
S. Ghione ◽  
C. Palombo ◽  
M. Pellegrini ◽  
E. Fommei ◽  
A. Pilo ◽  
...  
Keyword(s):  
Clearance Rate ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Metabolic Clearance ◽  
Venous Sampling ◽  
Metabolic Clearance Rate ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Endogenous Noradrenaline ◽  
Kinetics Of

1. The kinetics of plasma noradrenaline have been determined in normal and essential hypertensive patients by intravenous injection of tritiated noradrenaline and serial mixed venous sampling. 2. The metabolic clearance rate of plasma noradrenaline in normal subjects was approximately 1·1 min−1 m−2, whereas in essential hypertensive patients it was significantly reduced to approximately 0·61 min−1 m−2. 3. Metabolic clearance rate was negatively correlated to mean arterial blood pressure and total peripheral resistances. 4. Particularly low values of metabolic clearance rate were found in two patients with congestive heart failure and one with phaeochromocytoma. 5. We propose that the access of plasma noradrenaline to the main removal mechanisms takes place in competition with the flow of unlabelled endogenous noradrenaline directly released by nerve endings. The slower removal of plasma noradrenaline in essential hypertension could then express a larger release of endogenous noradrenaline in this condition.

Effect of phentolamine on the insulin, glucagon, and glucose responses to exercise in adrenal-denervated sheep

1985 ◽  
Vol 63 (4) ◽  
pp. 346-349 ◽  
Author(s):  
Ronald P. Brockman
Keyword(s):  
Sympathetic Innervation ◽  
Adrenergic Innervation ◽  
Metabolic Responses ◽  
Metabolic Clearance ◽  
Adrenergic Stimulation ◽  
Hepatic Glucose Output ◽  
Optimal Response ◽  
Hepatic Glucose ◽  
Alpha Blockade ◽  
Glucose Output

Hyperglycemia and increased hepatic glucose output are characteristic responses to exercise in sheep. They appear to be due in part to α-adrenergic stimulation. To delineate the contributions of sympathetic innervation and adrenal catecholamines to the hormonal and metabolic responses to exercise, adrenal-denervated sheep were exercised with and without α-blockade (phentolamine treatment). Alpha blockade exaggerated the hyperinsulinemia during exercise (increment of 61 ± 8 vs. 34 ± 7 μU/mL for the control). This was associated with a reduction in glucose appearance (increments of 63 ± 8 vs. 236 ± 23 μmol/min, respectively). The metabolic clearance rates were not altered by α-blockade. It appears that both the adrenal catecholamines and adrenergic innervation to the pancreas contribute to the prevention of a rise in insulin concentrations during exercise in sheep. While this may not be essential for glucose appearance to rise during exercise, it appears necessary for an optimal response.

scholarly journals Blood flow and nutrient exchange across the liver and gut of the dairy cow

1983 ◽  
Vol 49 (3) ◽  
pp. 481-496 ◽  
Author(s):  
M. A. Lomax ◽  
G. D. Baird
Keyword(s):  
Fatty Acids ◽  
Blood Flow ◽  
Flow Rate ◽  
Ketone Bodies ◽  
Blood Flow Rate ◽  
Hepatic Uptake ◽  
Hepatic Glucose Output ◽  
Lactating Cows ◽  
Hepatic Glucose ◽  
Glucose Output

1. The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting.2. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake.3. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptakes of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows.4. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine+threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting.5. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield.6. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

Measurement of hepatic glucose output and hepatic blood flow in response to glucagon

1959 ◽  
Vol 196 (2) ◽  
pp. 315-318 ◽  
Author(s):  
William C. Shoemaker ◽  
Theodore B. Van Itallie ◽  
William F. Walker
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Glucose Concentration ◽  
Base Line ◽  
Hepatic Glucose Output ◽  
Marked Rise ◽  
Hepatic Glucose ◽  
The Mean ◽  
Glucose Output ◽  
Venous Glucose

Arterial, portal and hepatic venous glucose concentrations and hepatic blood flow were simultaneously measured in nine dogs in the postabsorptive state, and after intravenous administration of glucagon. A marked rise in hepatic venous glucose concentration occurred promptly after glucagon administration. This rise coincided with a mean increase in estimated hepatic blood flow of approximately 100%. This increase in hepatic blood flow following the administration of glucagon was regularly observed in all animals; the increase in blood flow ranged from 41 to 204% in this series. Hepatic glucose output was calculated by multiplying the portal-hepatic vein gradient by the hepatic blood flow. The mean hepatic glucose output of the series increased from base line of 73 mg/min. to a maximum of 381 mg/min. in response to glucagon.

Catecholamine physiology in ovine fetus. II. Metabolic clearance rate of epinephrine

1984 ◽  
Vol 246 (4) ◽  
pp. E350-E355
Author(s):  
S. M. Palmer ◽  
G. K. Oakes ◽  
R. W. Lam ◽  
C. J. Hobel ◽  
D. A. Fisher
Keyword(s):  
Clearance Rate ◽  
Blood Gases ◽  
Constant Infusion ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Control Value ◽  
Fetal Plasma ◽  
Arterial Blood

This study measured the metabolic clearance rate (MCR) of epinephrine (E) in 13 chronically catheterized fetal lambs between 120 and 145 days gestation. The E-MCR was determined by a constant infusion method at an E infusion rate of 0.1 microgram/kg estimated fetal wt. Fetal and maternal arterial blood samples were taken for measurements of catecholamine levels, pH, blood gases, and glucose. There was a significant positive correlation between gestational age and E-MCR (r = 0.87, P less than 0.001). The E production rate in fetuses less than 132 days (n = 6) (1,234 +/- 301 pg/min) was not significantly different from fetuses greater than or equal to 132 days (n = 7) (1,195 +/- 242). Catecholamine infusion resulted in a decrease in pH from a control value of 7.37 +/- 0.01 to 7.31 +/- 0.01 by 15 min of infusion, but there were no significant changes in fetal heart rate or blood pressure. The mean fetal plasma glucose concentration increased 45% above base line at 15 and 20 min and 65% above base line by 30 min of catecholamine infusion. After 60 min of infusion plasma norepinephrine (NE) increased from 380 +/- 60 to 520 +/- 75 pg/ml and plasma dopamine from 100 +/- 20 to 240 +/- 50 pg/ml (both P less than 0.05). These results indicate that E-MCR increases with maturation in the absence of a change in basal E production.

Sign in / Sign up

Export Citation Format

Share Document